Cardiovascular Research Advance Access originally published online on May 2, 2008
Cardiovascular Research 2008 79(1):161-168; doi:10.1093/cvr/cvn111
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Cyclooxygenase-dependent vasoconstricting factor(s) in remodelled rat femoral arteries
1 Department of Clinical Pharmacology and Therapeutics, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, Shizuoka 431-3192, Japan
2 Department of Pharmacology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
3 Department of Clinical Pharmacology and Therapeutics, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama-machi, Yufu, Oita 879-5593, Japan
* Corresponding author. Tel: +81 53 435 2385; fax: +81 53 435 2384. E-mail address: hwat{at}hama-med.ac.jp
Aims: Denudation and regeneration of the vascular endothelium are important in the pathogenesis of atherosclerosis. The aim of this study is to clarify the mechanisms of functional alterations in remodelled arteries following endothelial injury.
Methods and results: Non-mechanical endothelial injury was induced by 540-nm light irradiation of rose Bengal in femoral arteries of Wistar rats. Endothelium-dependent vasodilation was assessed by the response to acetylcholine (ACh) 1, 2, and 4 weeks after the injury. In control arteries, ACh-induced relaxation was mainly nitric oxide-dependent at all study time points. In injured arteries, this response was completely restored at 1 week, but was more dependent on KCl-sensitive endothelium-derived hyperpolarizing factor production during the first 2 weeks. Cyclooxygenase (COX) isoforms 1 and 2 were detected in the endothelium of injured arteries, and inhibition of prostanoids production with the non-specific COX inhibitor indomethacin substantially enhanced the ACh-induced vasorelaxation response in injured arteries, but did not affect control arteries. Similar effects were observed with the COX-1 inhibitor SC-560, the COX-2 inhibitor NS-398, the thromboxane (TX) A2/prostaglandin (PG) H2 receptor antagonist SQ29548 and the PGF2
receptor antagonist AL-8810. However, the TX synthetase inhibitor OKY-046 had no effect on ACh-induced relaxation in injured arteries.
Conclusion: In remodelled arteries following photochemical endothelial injury, the vasoconstrictive prostanoids PGH2 and PGF2
, but not TXA2, contribute to changes in endothelium-dependent vascular response via COX-1- and 2-dependent pathways.
KEYWORDS Endothelium; Cyclooxygenase; Vasoconstricting factor(s); Remodeling; Prostanoids
Time for primary review: 25 days
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
K. Schror Cyclooxygenase-2-Derived Prostaglandin F2{alpha}: An Endothelium-Derived Contractile Factor Acting Independently of Other Endothelium-Derived Contractile Factors via Vascular Thromboxane Receptors Circ. Res., January 30, 2009; 104(2): 141 - 143. [Full Text] [PDF] |
||||
![]() |
P. M. Vanhoutte and E. H. C. Tang Endothelium-dependent contractions: when a good guy turns bad! J. Physiol., November 15, 2008; 586(22): 5295 - 5304. [Abstract] [Full Text] [PDF] |
||||

